Abstract

We have examined the possibility that human polymorphonuclear cells exposed to IgA immune complexes can mediate the production of platelet-activating factor (PAF) and oxygen radicals. We found that human IgA and IgG immune aggregates stimulated, to a similar extent, PAF and O2- production by human polymorphonuclear cells (PMN) in a concentration and time dependent manner. The PAF, that was largely associated with cells, was shown to be identical to synthetic PAF, as determined by physicochemical, chromatographic and enzymatic assay. Furthermore, de novo synthesis of PAF by PMN was shown to occur by incorporation of radioactive precursors, such as [3H]acetate. The addition of normal human serum to PMN incubated with IgG aggregates resulted in a significant amount of PAF formation which was not observed with IgA aggregates. By contrast, no change was seen in PMN O2- with either aggregates. The preincubation of PMN with cytochalasin B, an inhibitor of phagocytosis, did not affect PAF and O2- production by both aggregates. The results suggest that the interaction of PMN with the IgA complexes in blood vessel walls of different tissues can result in the release of lipid mediators, such as PAF and oxygen radicals that could contribute to the inflammatory response.

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